#neuroplasticity — Public Fediverse posts
Live and recent posts from across the Fediverse tagged #neuroplasticity, aggregated by home.social.
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Scientists start to understand how stressed children’s brains develop. Could this explain the effect ketamine has on neuroplasticity? medicalnewsbulletin.com/critical-per... 🧪 🧠 #ketamine #childdevelopment #neuroplasticity
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#PersonalGrowth #PersonalGrowth #SelfImprovement #Mindset #Transformation #InnerPeace #SelfAwareness #Consciousness #Motivation #Inspiration #Neuro#NeuroScience #NeuroPlasticity #NeuroDivergent #NeuroCiencia #NeuroCirurgia #NeuroDiverse #NeuroFeedback #Wellbeing https://mastodon.social/@biohackingpathway/117330662743894606
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DATE: September 21, 2026 at 09:49PM
SOURCE: SCIENCE DAILY MIND-BRAIN FEEDTITLE: Stem cells reverse stroke damage and restore movement in mice
URL: https://www.sciencedaily.com/releases/2026/09/260921081116.htm
Stem cell transplants helped regenerate stroke-damaged brain tissue in mice, producing new neurons and restoring lost motor function. The treatment also improved blood vessels, inflammation, and the blood-brain barrier, raising hopes that a similar approach could eventually help repair the human brain after stroke.
URL: https://www.sciencedaily.com/releases/2026/09/260921081116.htm
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Private, vetted email list for mental health professionals: https://www.clinicians-exchange.org
Unofficial Psychology Today Xitter to toot feed at Psych Today Unofficial Bot @PTUnofficialBot
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#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #StemCells #StrokeRecovery #BrainRegeneration #NeuroScience #MotorFunction #MiceStudy #Neuroplasticity #BloodBrainBarrier #RegenerativeMedicine #StrokeResearch
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DATE: September 21, 2026 at 09:49PM
SOURCE: SCIENCE DAILY MIND-BRAIN FEEDTITLE: Stem cells reverse stroke damage and restore movement in mice
URL: https://www.sciencedaily.com/releases/2026/09/260921081116.htm
Stem cell transplants helped regenerate stroke-damaged brain tissue in mice, producing new neurons and restoring lost motor function. The treatment also improved blood vessels, inflammation, and the blood-brain barrier, raising hopes that a similar approach could eventually help repair the human brain after stroke.
URL: https://www.sciencedaily.com/releases/2026/09/260921081116.htm
-------------------------------------------------
Private, vetted email list for mental health professionals: https://www.clinicians-exchange.org
Unofficial Psychology Today Xitter to toot feed at Psych Today Unofficial Bot @PTUnofficialBot
-------------------------------------------------
#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #StemCells #StrokeRecovery #BrainRegeneration #NeuroScience #MotorFunction #MiceStudy #Neuroplasticity #BloodBrainBarrier #RegenerativeMedicine #StrokeResearch
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DATE: September 21, 2026 at 09:49PM
SOURCE: SCIENCE DAILY MIND-BRAIN FEEDTITLE: Stem cells reverse stroke damage and restore movement in mice
URL: https://www.sciencedaily.com/releases/2026/09/260921081116.htm
Stem cell transplants helped regenerate stroke-damaged brain tissue in mice, producing new neurons and restoring lost motor function. The treatment also improved blood vessels, inflammation, and the blood-brain barrier, raising hopes that a similar approach could eventually help repair the human brain after stroke.
URL: https://www.sciencedaily.com/releases/2026/09/260921081116.htm
-------------------------------------------------
Private, vetted email list for mental health professionals: https://www.clinicians-exchange.org
Unofficial Psychology Today Xitter to toot feed at Psych Today Unofficial Bot @PTUnofficialBot
-------------------------------------------------
#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #StemCells #StrokeRecovery #BrainRegeneration #NeuroScience #MotorFunction #MiceStudy #Neuroplasticity #BloodBrainBarrier #RegenerativeMedicine #StrokeResearch
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DATE: September 18, 2026 at 02:00PM
SOURCE: PSYPOST.ORG** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
-------------------------------------------------TITLE: Do antidepressants actually alter brain structure? A massive neuroscience study weighs in
A massive brain imaging study has found that subtle differences in the brain structure of people taking antidepressants are largely explained by the severity of their depression, rather than the medications themselves. The research also suggests that the relationship between depression, medication use, and brain anatomy changes across a person’s lifespan, with younger patients showing distinct structural patterns. The findings were published in Molecular Psychiatry.
Major depressive disorder is a severe and persistent form of depression that ranks among the leading causes of disability worldwide. To treat it, doctors frequently prescribe antidepressant medications, yet the exact biological mechanisms by which these drugs alter the brain remain somewhat elusive.
A 2006 theoretical framework proposed that chronic stress and depression might damage brain cells, and that antidepressants could stimulate the growth of new cells in deep brain regions. Supporting this idea, a study covered by PsyPost in 2026 indicated that treatments like duloxetine could help normalize the microscopic structure of brain tissue in depressed patients, whereas those given a placebo saw their brain tissue drift further from healthy levels.
To investigate these effects on a larger scale, researchers needed massive datasets. In prior work, the ENIGMA consortium, an international network of brain researchers, mapped how depression physically alters the brain. For instance, a 2015 study from the group found that people with major depression tend to have a smaller hippocampus, which is a seahorse-shaped structure deep in the brain that plays a primary role in memory and emotion.
Building on this lineage, researchers analyzed data from this same international network to see if antidepressant use actually counteracts these structural brain changes, and whether those effects differ depending on a patient’s age and sex.
“In several of our previous large international ENIGMA studies of depression, we kept seeing an intriguing pattern: the most widespread brain differences were often found in people with depression who were taking antidepressants at the time of their brain scan,” Lianne Schmaal, head of Mood & Anxiety Disorders Research and chair of the ENIGMA MDD consortium at Orygen and the Centre for Youth Mental Health at The University of Melbourne, told PsyPost.
“We wanted to understand that pattern better,” Schmaal explained. “Our earlier studies did not have sufficiently detailed information about how long people had been taking antidepressants or which type they were taking, and they could not tell us whether the differences we observed were related to the medication itself or to the reasons people were taking medication in the first place.”
To answer these questions, Schmaal, lead author Chaira Serrarens, and their colleagues pooled data from 32 different international cohorts, yielding a total sample of 8,696 individuals. This massive group was divided into three categories: 2,076 people with major depressive disorder who were currently taking antidepressants, 1,495 people with the disorder who were not taking antidepressants, and 5,125 healthy controls with no history of the condition.
“One of the strengths of this study is its scale,” Schmaal said. “By bringing together almost 8,700 people from 32 research cohorts around the world and analyzing their brain scans using harmonized methods, we could identify subtle patterns that smaller studies would struggle to detect reliably.”
All participants underwent structural magnetic resonance imaging (MRI), a technique that uses strong magnetic fields and radio waves to create highly detailed, three-dimensional pictures of brain anatomy. The researchers processed these brain scans using automated software to measure three main things. First, they measured the thickness of the cerebral cortex, which is the wrinkled outer layer of the brain responsible for higher-level thinking and processing. Second, they measured the total surface area of this outer layer. Third, they measured the volume of subcortical structures, which are the specialized hubs located deep beneath the outer cortex.
To ensure a fair comparison, the statistical models accounted for the participants’ age, sex, and total head size. The researchers also gathered clinical data from the depressed patients, including the severity of their current symptoms based on standard psychological questionnaires, their number of past depressive episodes, and, for a smaller subset, the specific type of antidepressant they were taking.
The brain scans revealed a complex relationship between age, medication status, and brain structure. For example, younger individuals in the medicated group (those under 50 years old) showed a thinner middle temporal gyrus compared to both the unmedicated patients and the healthy controls. The middle temporal gyrus is a ridge on the side of the brain involved in processing sensory information and emotional cues. In older individuals, this difference between the groups disappeared, with the lines crossing over around age 50.
“One of the most interesting findings was that age seemed to matter,” Schmaal noted. “Some of the differences associated with antidepressant use were most apparent in younger people and were not seen in the same way in older adults. That suggests we should not necessarily assume that the relationship between antidepressant treatment and the brain is the same across the lifespan.”
When looking at the overall effects of medication regardless of age, the researchers found that patients currently taking antidepressants had a smaller hippocampus and a thinner inferior temporal gyrus compared to patients who were not taking the drugs. The researchers ran extra tests to see if these differences were simply due to the medicated patients having a longer or more stubborn history of depression. The structural differences held true even when adjusting for the number of past depressive episodes or whether the patient was currently in remission.
However, the researchers caution that these alterations are not glaringly obvious on an individual level. “The differences were small,” Schmaal told PsyPost. “They are detectable because we were able to combine data from thousands of people, but they are nowhere near large enough to look at an individual person’s brain scan and determine whether they have taken antidepressants, or to use these measures in clinical decision-making.”
The differences between the medicated and unmedicated groups also vanished when the researchers accounted for the severity of current depressive symptoms. The people in the medicated group generally reported feeling worse at the time of the scan than the unmedicated group. This indicates that the structural differences in the temporal lobe and hippocampus might be tied more to how severely depressed a person is currently feeling, rather than being a direct physical result of the medication itself.
“We tried to account for factors such as current symptoms, number of previous depressive episodes and whether someone had recurrent depression, but it is impossible to completely separate medication use from illness severity in this kind of study,” Schmaal explained.
“Despite exploring every possible difference between those taking and those not taking antidepressants, there were only very small differences in very few brain areas which disappeared when taking into account other important differences between these groups,” Roland Zahn, a professor of Mood Disorders and Cognitive Neuroscience at King’s College London’s Centre for Affective Disorders who was not involved in the research, told PsyPost.
Zahn, who also serves as co-programme lead for the MSc Affective Disorders and shares research updates via his lab blog, added: “One important difference between the groups was that people taking antidepressants had much higher levels of depressive symptoms as measured on a gold standard observer-rated scale known to correlate with subtle changes in brain structure from other studies. When accounting for this crucial difference between the groups, the subtle differences in thickness of some of the brain areas in those taking antidepressants disappeared.”
The study also highlighted brain changes that seem driven by the depression diagnosis itself rather than the medication. Younger patients with depression, regardless of whether they took medication, had a smaller thalamus compared to healthy controls. The thalamus acts as a central relay station for sensory and motor signals in the brain. These younger patients also exhibited a thinner cortex in several regions across the frontal, occipital, and parietal lobes when compared to healthy individuals, a gap that was not present in the older participants.
In a smaller exploratory analysis, the researchers looked at specific types of antidepressants, comparing selective serotonin reuptake inhibitors (SSRIs), serotonin-norepinephrine reuptake inhibitors (SNRIs), and mirtazapine. They found an age-specific pattern here as well. Older adults (over the age of 40) taking mirtazapine had a thicker rostral anterior cingulate cortex compared to older adults taking SSRIs or SNRIs.
This brain region sits in the frontal lobe and is heavily involved in emotional regulation and reward processing. The authors suggest that mirtazapine might trigger a distinct neuroplastic response in this area, though they also note that mirtazapine is often prescribed for specific symptoms like insomnia or after other drugs have failed, which might influence the results.
“The authors acknowledge that they cannot establish causal relationships and particularly their comparison of different antidepressants is exploratory and based on a much smaller group, based on a single time point,” Zahn noted. “The problem is that there are several factors influencing the reason why someone is taking one antidepressant rather than another and the authors acknowledge, they were not able to account for that as this is a large study with limited clinical background information.”
The researchers also investigated how long patients had been on their current medication, finding no clear association between duration of use and structural changes. “We also did not find evidence that a longer duration of current antidepressant use was associated with greater brain differences,” Schmaal said. “That is reassuring in one sense, but it needs to be interpreted cautiously because detailed information on duration was available for only a subset of participants, and importantly we did not have people’s complete lifetime history of antidepressant exposure.”
The findings are in tension with research covered by PsyPost earlier this year, which found that patients taking the antidepressant escitalopram experienced increases in right hippocampal volume during their treatment. Both studies measure hippocampal volume via MRI in depressed patients taking antidepressants, but that earlier study tracked longitudinal within-person volume changes over weeks of treatment, whereas the new study assessed cross-sectional volume differences between different groups of medicated and unmedicated patients at a single point in time.
However, the ENIGMA study’s immense size adds significant weight to its findings. “This is a very important study in that it was able to merge data from thousands of people and therefore had the ability to detect very small differences,” Zahn said. “It thereby challenged findings from non-human animals as well as findings in smaller studies.”
As with all research, there are a few things to keep in mind. The study relies on a cross-sectional design, meaning the participants were only scanned once. Because the researchers did not track the same individuals over time, they cannot definitively say whether the antidepressants caused the observed brain differences, or if people with certain brain shapes and symptom severities are simply more likely to be prescribed antidepressants.
“The main misinterpretation I would want to avoid is that this study shows antidepressants cause the brain to shrink or cause brain damage. It does not,” Schmaal said. “Imagine taking a photograph of two groups of people today: one group taking antidepressants and another group not taking them. Even if their brains differ on average, that photograph cannot tell you what caused the difference or what their brains looked like before treatment.”
Zahn echoed this caution, emphasizing that brain anatomy is highly variable. “It is also important to note that the structure of our brains constantly changes and the biggest driver of such change is age,” he said. “It is also important to note that large individual differences in brain structure exist with little impact on functioning.”
Because of this limitation, the findings should not alter how patients currently manage their condition. “That is why these results should not be used to make decisions about starting or stopping antidepressants,” Schmaal added. “Those decisions need to be based on the balance of benefits and risks for an individual person and discussed with their treating clinician.”
The researchers also lacked data on the participants’ lifetime history of medication use, meaning some people in the “unmedicated” group might have taken antidepressants in the past. Other factors that shape brain anatomy over a lifespan, such as education, lifestyle habits, or early signs of neurodegenerative diseases in older adults, could not be fully accounted for across all 32 international sites.
“The next critical step is longitudinal research,” Schmaal told PsyPost. “Ideally, we need to follow people from before, or very soon after, they first start an antidepressant and repeatedly assess both their mental health and their brain over several years.”
“The next step as the authors acknowledge is to investigate multiple time points in datasets which contain more detail about other relevant factors, such as other conditions, and response to previous treatments,” Zahn added.
“Ultimately, the goal is not simply to ask whether antidepressants affect the brain,” Schmaal concluded. “We want to understand how they affect the developing and adult brain, whether those effects differ between individuals and across different ages, and whether any brain changes relate to treatment benefit, side effects or longer-term outcomes.”
The study, “Regional brain morphology and current antidepressant use: findings from 32 international cohorts from the ENIGMA major depressive disorder working group,” was authored by Chaira Serrarens, Yara J. Toenders, Elena Pozzi, André Aleman, Nina Alexander, Zeynep Başgöze, Vladimir Belov, Klaus Berger, Katharina Brosch, Robin Bülow, Geraldo Filho Busatto, Liliana P. Capitão, Colm G. Connolly, Baptiste Couvy-Duchesne, Kathryn R. Cullen, Udo Dannlowski, Christopher G. Davey, Greig I. de Zubicaray, Danai Dima, Katharina Dohm, Verena Enneking, Tracy Erwin-Grabner, Ulrika Evermann, Cynthia H. Y. Fu, Paola Fuentes-Claramonte, Beata R. Godlewska, Ali Saffet Gonul, Ian H. Gotlib, Roberto Goya-Maldonado, Hans J. Grabe, Nynke A. Groenewold, Dominik Grotegerd, Oliver Gruber, Tim Hahn, Geoffrey Hall, Ben J. Harrison, Walter Heindel, Marco Hermesdorf, Tiffany C. Ho, Naho Ichikawa, Eri Itai, Neda Jahanshad, Hamidreza Jamalabadi, Alec J. Jamieson, Andreas Jansen, Tilo Kircher, Bonnie Klimes-Dougan, Bernd Krämer, Axel Krug, Thomas M. Lancaster, Elisabeth J. Leehr, Meng Li, David E. J. Linden, Frank MacMaster, Katie L. McMahon, Sarah E. Medland, David M. A. Mehler, Susanne Meinert, Benson Mwangi, Igor Nenadić, Go Okada, Yasumasa Okamoto, Nils Opel, Julia-Katharina Pfarr, Edith Pomarol-Clotet, Maria J. Portella, Ronny Redlich, Liesbeth Reneman, Jonathan Repple, Kai Ringwald, Elena Rodriguez-Cano, Pedro G. P. Rosa, Matthew D. Sacchet, Philipp G. Sämann, Raymond Salvador, Anouk Schrantee, Hotaka Shinzato, Kang Sim, Egle Simulionyte, Jair C. Soares, Dan J. Stein, Frederike Stein, Benjamin Straube, Lachlan T. Strike, Florian Thomas-Odenthal, Sophia I. Thomopoulos, Paul M. Thompson, Marie-Jose van Tol, Paula Usemann, Aslihan Uyar, Nic van der Wee, Steven van der Werff, Yolanda Vives-Gilabert, Henry Völzke, Martin Walter, Sarah Whittle, Katharina Wittfeld, Adrian Wroblewski, Mon-Ju Wu, Tony T. Yang, Giovana B. Zunta-Soares, Dick J. Veltman, Lianne Schmaal, and Laura S. van Velzen.
-------------------------------------------------
Private, vetted email list for mental health professionals: https://www.clinicians-exchange.org
Unofficial Psychology Today Xitter to toot feed at Psych Today Unofficial Bot @PTUnofficialBot
-------------------------------------------------
#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #antidepressants #brainstructure #ENIGMA #MDD #hippocampus #neuroimaging #MolecularPsychiatry #depressionresearch #lifespan #neuroplasticity
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DATE: September 18, 2026 at 02:00PM
SOURCE: PSYPOST.ORG** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
-------------------------------------------------TITLE: Do antidepressants actually alter brain structure? A massive neuroscience study weighs in
A massive brain imaging study has found that subtle differences in the brain structure of people taking antidepressants are largely explained by the severity of their depression, rather than the medications themselves. The research also suggests that the relationship between depression, medication use, and brain anatomy changes across a person’s lifespan, with younger patients showing distinct structural patterns. The findings were published in Molecular Psychiatry.
Major depressive disorder is a severe and persistent form of depression that ranks among the leading causes of disability worldwide. To treat it, doctors frequently prescribe antidepressant medications, yet the exact biological mechanisms by which these drugs alter the brain remain somewhat elusive.
A 2006 theoretical framework proposed that chronic stress and depression might damage brain cells, and that antidepressants could stimulate the growth of new cells in deep brain regions. Supporting this idea, a study covered by PsyPost in 2026 indicated that treatments like duloxetine could help normalize the microscopic structure of brain tissue in depressed patients, whereas those given a placebo saw their brain tissue drift further from healthy levels.
To investigate these effects on a larger scale, researchers needed massive datasets. In prior work, the ENIGMA consortium, an international network of brain researchers, mapped how depression physically alters the brain. For instance, a 2015 study from the group found that people with major depression tend to have a smaller hippocampus, which is a seahorse-shaped structure deep in the brain that plays a primary role in memory and emotion.
Building on this lineage, researchers analyzed data from this same international network to see if antidepressant use actually counteracts these structural brain changes, and whether those effects differ depending on a patient’s age and sex.
“In several of our previous large international ENIGMA studies of depression, we kept seeing an intriguing pattern: the most widespread brain differences were often found in people with depression who were taking antidepressants at the time of their brain scan,” Lianne Schmaal, head of Mood & Anxiety Disorders Research and chair of the ENIGMA MDD consortium at Orygen and the Centre for Youth Mental Health at The University of Melbourne, told PsyPost.
“We wanted to understand that pattern better,” Schmaal explained. “Our earlier studies did not have sufficiently detailed information about how long people had been taking antidepressants or which type they were taking, and they could not tell us whether the differences we observed were related to the medication itself or to the reasons people were taking medication in the first place.”
To answer these questions, Schmaal, lead author Chaira Serrarens, and their colleagues pooled data from 32 different international cohorts, yielding a total sample of 8,696 individuals. This massive group was divided into three categories: 2,076 people with major depressive disorder who were currently taking antidepressants, 1,495 people with the disorder who were not taking antidepressants, and 5,125 healthy controls with no history of the condition.
“One of the strengths of this study is its scale,” Schmaal said. “By bringing together almost 8,700 people from 32 research cohorts around the world and analyzing their brain scans using harmonized methods, we could identify subtle patterns that smaller studies would struggle to detect reliably.”
All participants underwent structural magnetic resonance imaging (MRI), a technique that uses strong magnetic fields and radio waves to create highly detailed, three-dimensional pictures of brain anatomy. The researchers processed these brain scans using automated software to measure three main things. First, they measured the thickness of the cerebral cortex, which is the wrinkled outer layer of the brain responsible for higher-level thinking and processing. Second, they measured the total surface area of this outer layer. Third, they measured the volume of subcortical structures, which are the specialized hubs located deep beneath the outer cortex.
To ensure a fair comparison, the statistical models accounted for the participants’ age, sex, and total head size. The researchers also gathered clinical data from the depressed patients, including the severity of their current symptoms based on standard psychological questionnaires, their number of past depressive episodes, and, for a smaller subset, the specific type of antidepressant they were taking.
The brain scans revealed a complex relationship between age, medication status, and brain structure. For example, younger individuals in the medicated group (those under 50 years old) showed a thinner middle temporal gyrus compared to both the unmedicated patients and the healthy controls. The middle temporal gyrus is a ridge on the side of the brain involved in processing sensory information and emotional cues. In older individuals, this difference between the groups disappeared, with the lines crossing over around age 50.
“One of the most interesting findings was that age seemed to matter,” Schmaal noted. “Some of the differences associated with antidepressant use were most apparent in younger people and were not seen in the same way in older adults. That suggests we should not necessarily assume that the relationship between antidepressant treatment and the brain is the same across the lifespan.”
When looking at the overall effects of medication regardless of age, the researchers found that patients currently taking antidepressants had a smaller hippocampus and a thinner inferior temporal gyrus compared to patients who were not taking the drugs. The researchers ran extra tests to see if these differences were simply due to the medicated patients having a longer or more stubborn history of depression. The structural differences held true even when adjusting for the number of past depressive episodes or whether the patient was currently in remission.
However, the researchers caution that these alterations are not glaringly obvious on an individual level. “The differences were small,” Schmaal told PsyPost. “They are detectable because we were able to combine data from thousands of people, but they are nowhere near large enough to look at an individual person’s brain scan and determine whether they have taken antidepressants, or to use these measures in clinical decision-making.”
The differences between the medicated and unmedicated groups also vanished when the researchers accounted for the severity of current depressive symptoms. The people in the medicated group generally reported feeling worse at the time of the scan than the unmedicated group. This indicates that the structural differences in the temporal lobe and hippocampus might be tied more to how severely depressed a person is currently feeling, rather than being a direct physical result of the medication itself.
“We tried to account for factors such as current symptoms, number of previous depressive episodes and whether someone had recurrent depression, but it is impossible to completely separate medication use from illness severity in this kind of study,” Schmaal explained.
“Despite exploring every possible difference between those taking and those not taking antidepressants, there were only very small differences in very few brain areas which disappeared when taking into account other important differences between these groups,” Roland Zahn, a professor of Mood Disorders and Cognitive Neuroscience at King’s College London’s Centre for Affective Disorders who was not involved in the research, told PsyPost.
Zahn, who also serves as co-programme lead for the MSc Affective Disorders and shares research updates via his lab blog, added: “One important difference between the groups was that people taking antidepressants had much higher levels of depressive symptoms as measured on a gold standard observer-rated scale known to correlate with subtle changes in brain structure from other studies. When accounting for this crucial difference between the groups, the subtle differences in thickness of some of the brain areas in those taking antidepressants disappeared.”
The study also highlighted brain changes that seem driven by the depression diagnosis itself rather than the medication. Younger patients with depression, regardless of whether they took medication, had a smaller thalamus compared to healthy controls. The thalamus acts as a central relay station for sensory and motor signals in the brain. These younger patients also exhibited a thinner cortex in several regions across the frontal, occipital, and parietal lobes when compared to healthy individuals, a gap that was not present in the older participants.
In a smaller exploratory analysis, the researchers looked at specific types of antidepressants, comparing selective serotonin reuptake inhibitors (SSRIs), serotonin-norepinephrine reuptake inhibitors (SNRIs), and mirtazapine. They found an age-specific pattern here as well. Older adults (over the age of 40) taking mirtazapine had a thicker rostral anterior cingulate cortex compared to older adults taking SSRIs or SNRIs.
This brain region sits in the frontal lobe and is heavily involved in emotional regulation and reward processing. The authors suggest that mirtazapine might trigger a distinct neuroplastic response in this area, though they also note that mirtazapine is often prescribed for specific symptoms like insomnia or after other drugs have failed, which might influence the results.
“The authors acknowledge that they cannot establish causal relationships and particularly their comparison of different antidepressants is exploratory and based on a much smaller group, based on a single time point,” Zahn noted. “The problem is that there are several factors influencing the reason why someone is taking one antidepressant rather than another and the authors acknowledge, they were not able to account for that as this is a large study with limited clinical background information.”
The researchers also investigated how long patients had been on their current medication, finding no clear association between duration of use and structural changes. “We also did not find evidence that a longer duration of current antidepressant use was associated with greater brain differences,” Schmaal said. “That is reassuring in one sense, but it needs to be interpreted cautiously because detailed information on duration was available for only a subset of participants, and importantly we did not have people’s complete lifetime history of antidepressant exposure.”
The findings are in tension with research covered by PsyPost earlier this year, which found that patients taking the antidepressant escitalopram experienced increases in right hippocampal volume during their treatment. Both studies measure hippocampal volume via MRI in depressed patients taking antidepressants, but that earlier study tracked longitudinal within-person volume changes over weeks of treatment, whereas the new study assessed cross-sectional volume differences between different groups of medicated and unmedicated patients at a single point in time.
However, the ENIGMA study’s immense size adds significant weight to its findings. “This is a very important study in that it was able to merge data from thousands of people and therefore had the ability to detect very small differences,” Zahn said. “It thereby challenged findings from non-human animals as well as findings in smaller studies.”
As with all research, there are a few things to keep in mind. The study relies on a cross-sectional design, meaning the participants were only scanned once. Because the researchers did not track the same individuals over time, they cannot definitively say whether the antidepressants caused the observed brain differences, or if people with certain brain shapes and symptom severities are simply more likely to be prescribed antidepressants.
“The main misinterpretation I would want to avoid is that this study shows antidepressants cause the brain to shrink or cause brain damage. It does not,” Schmaal said. “Imagine taking a photograph of two groups of people today: one group taking antidepressants and another group not taking them. Even if their brains differ on average, that photograph cannot tell you what caused the difference or what their brains looked like before treatment.”
Zahn echoed this caution, emphasizing that brain anatomy is highly variable. “It is also important to note that the structure of our brains constantly changes and the biggest driver of such change is age,” he said. “It is also important to note that large individual differences in brain structure exist with little impact on functioning.”
Because of this limitation, the findings should not alter how patients currently manage their condition. “That is why these results should not be used to make decisions about starting or stopping antidepressants,” Schmaal added. “Those decisions need to be based on the balance of benefits and risks for an individual person and discussed with their treating clinician.”
The researchers also lacked data on the participants’ lifetime history of medication use, meaning some people in the “unmedicated” group might have taken antidepressants in the past. Other factors that shape brain anatomy over a lifespan, such as education, lifestyle habits, or early signs of neurodegenerative diseases in older adults, could not be fully accounted for across all 32 international sites.
“The next critical step is longitudinal research,” Schmaal told PsyPost. “Ideally, we need to follow people from before, or very soon after, they first start an antidepressant and repeatedly assess both their mental health and their brain over several years.”
“The next step as the authors acknowledge is to investigate multiple time points in datasets which contain more detail about other relevant factors, such as other conditions, and response to previous treatments,” Zahn added.
“Ultimately, the goal is not simply to ask whether antidepressants affect the brain,” Schmaal concluded. “We want to understand how they affect the developing and adult brain, whether those effects differ between individuals and across different ages, and whether any brain changes relate to treatment benefit, side effects or longer-term outcomes.”
The study, “Regional brain morphology and current antidepressant use: findings from 32 international cohorts from the ENIGMA major depressive disorder working group,” was authored by Chaira Serrarens, Yara J. Toenders, Elena Pozzi, André Aleman, Nina Alexander, Zeynep Başgöze, Vladimir Belov, Klaus Berger, Katharina Brosch, Robin Bülow, Geraldo Filho Busatto, Liliana P. Capitão, Colm G. Connolly, Baptiste Couvy-Duchesne, Kathryn R. Cullen, Udo Dannlowski, Christopher G. Davey, Greig I. de Zubicaray, Danai Dima, Katharina Dohm, Verena Enneking, Tracy Erwin-Grabner, Ulrika Evermann, Cynthia H. Y. Fu, Paola Fuentes-Claramonte, Beata R. Godlewska, Ali Saffet Gonul, Ian H. Gotlib, Roberto Goya-Maldonado, Hans J. Grabe, Nynke A. Groenewold, Dominik Grotegerd, Oliver Gruber, Tim Hahn, Geoffrey Hall, Ben J. Harrison, Walter Heindel, Marco Hermesdorf, Tiffany C. Ho, Naho Ichikawa, Eri Itai, Neda Jahanshad, Hamidreza Jamalabadi, Alec J. Jamieson, Andreas Jansen, Tilo Kircher, Bonnie Klimes-Dougan, Bernd Krämer, Axel Krug, Thomas M. Lancaster, Elisabeth J. Leehr, Meng Li, David E. J. Linden, Frank MacMaster, Katie L. McMahon, Sarah E. Medland, David M. A. Mehler, Susanne Meinert, Benson Mwangi, Igor Nenadić, Go Okada, Yasumasa Okamoto, Nils Opel, Julia-Katharina Pfarr, Edith Pomarol-Clotet, Maria J. Portella, Ronny Redlich, Liesbeth Reneman, Jonathan Repple, Kai Ringwald, Elena Rodriguez-Cano, Pedro G. P. Rosa, Matthew D. Sacchet, Philipp G. Sämann, Raymond Salvador, Anouk Schrantee, Hotaka Shinzato, Kang Sim, Egle Simulionyte, Jair C. Soares, Dan J. Stein, Frederike Stein, Benjamin Straube, Lachlan T. Strike, Florian Thomas-Odenthal, Sophia I. Thomopoulos, Paul M. Thompson, Marie-Jose van Tol, Paula Usemann, Aslihan Uyar, Nic van der Wee, Steven van der Werff, Yolanda Vives-Gilabert, Henry Völzke, Martin Walter, Sarah Whittle, Katharina Wittfeld, Adrian Wroblewski, Mon-Ju Wu, Tony T. Yang, Giovana B. Zunta-Soares, Dick J. Veltman, Lianne Schmaal, and Laura S. van Velzen.
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DATE: September 18, 2026 at 02:00PM
SOURCE: PSYPOST.ORG** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
-------------------------------------------------TITLE: Do antidepressants actually alter brain structure? A massive neuroscience study weighs in
A massive brain imaging study has found that subtle differences in the brain structure of people taking antidepressants are largely explained by the severity of their depression, rather than the medications themselves. The research also suggests that the relationship between depression, medication use, and brain anatomy changes across a person’s lifespan, with younger patients showing distinct structural patterns. The findings were published in Molecular Psychiatry.
Major depressive disorder is a severe and persistent form of depression that ranks among the leading causes of disability worldwide. To treat it, doctors frequently prescribe antidepressant medications, yet the exact biological mechanisms by which these drugs alter the brain remain somewhat elusive.
A 2006 theoretical framework proposed that chronic stress and depression might damage brain cells, and that antidepressants could stimulate the growth of new cells in deep brain regions. Supporting this idea, a study covered by PsyPost in 2026 indicated that treatments like duloxetine could help normalize the microscopic structure of brain tissue in depressed patients, whereas those given a placebo saw their brain tissue drift further from healthy levels.
To investigate these effects on a larger scale, researchers needed massive datasets. In prior work, the ENIGMA consortium, an international network of brain researchers, mapped how depression physically alters the brain. For instance, a 2015 study from the group found that people with major depression tend to have a smaller hippocampus, which is a seahorse-shaped structure deep in the brain that plays a primary role in memory and emotion.
Building on this lineage, researchers analyzed data from this same international network to see if antidepressant use actually counteracts these structural brain changes, and whether those effects differ depending on a patient’s age and sex.
“In several of our previous large international ENIGMA studies of depression, we kept seeing an intriguing pattern: the most widespread brain differences were often found in people with depression who were taking antidepressants at the time of their brain scan,” Lianne Schmaal, head of Mood & Anxiety Disorders Research and chair of the ENIGMA MDD consortium at Orygen and the Centre for Youth Mental Health at The University of Melbourne, told PsyPost.
“We wanted to understand that pattern better,” Schmaal explained. “Our earlier studies did not have sufficiently detailed information about how long people had been taking antidepressants or which type they were taking, and they could not tell us whether the differences we observed were related to the medication itself or to the reasons people were taking medication in the first place.”
To answer these questions, Schmaal, lead author Chaira Serrarens, and their colleagues pooled data from 32 different international cohorts, yielding a total sample of 8,696 individuals. This massive group was divided into three categories: 2,076 people with major depressive disorder who were currently taking antidepressants, 1,495 people with the disorder who were not taking antidepressants, and 5,125 healthy controls with no history of the condition.
“One of the strengths of this study is its scale,” Schmaal said. “By bringing together almost 8,700 people from 32 research cohorts around the world and analyzing their brain scans using harmonized methods, we could identify subtle patterns that smaller studies would struggle to detect reliably.”
All participants underwent structural magnetic resonance imaging (MRI), a technique that uses strong magnetic fields and radio waves to create highly detailed, three-dimensional pictures of brain anatomy. The researchers processed these brain scans using automated software to measure three main things. First, they measured the thickness of the cerebral cortex, which is the wrinkled outer layer of the brain responsible for higher-level thinking and processing. Second, they measured the total surface area of this outer layer. Third, they measured the volume of subcortical structures, which are the specialized hubs located deep beneath the outer cortex.
To ensure a fair comparison, the statistical models accounted for the participants’ age, sex, and total head size. The researchers also gathered clinical data from the depressed patients, including the severity of their current symptoms based on standard psychological questionnaires, their number of past depressive episodes, and, for a smaller subset, the specific type of antidepressant they were taking.
The brain scans revealed a complex relationship between age, medication status, and brain structure. For example, younger individuals in the medicated group (those under 50 years old) showed a thinner middle temporal gyrus compared to both the unmedicated patients and the healthy controls. The middle temporal gyrus is a ridge on the side of the brain involved in processing sensory information and emotional cues. In older individuals, this difference between the groups disappeared, with the lines crossing over around age 50.
“One of the most interesting findings was that age seemed to matter,” Schmaal noted. “Some of the differences associated with antidepressant use were most apparent in younger people and were not seen in the same way in older adults. That suggests we should not necessarily assume that the relationship between antidepressant treatment and the brain is the same across the lifespan.”
When looking at the overall effects of medication regardless of age, the researchers found that patients currently taking antidepressants had a smaller hippocampus and a thinner inferior temporal gyrus compared to patients who were not taking the drugs. The researchers ran extra tests to see if these differences were simply due to the medicated patients having a longer or more stubborn history of depression. The structural differences held true even when adjusting for the number of past depressive episodes or whether the patient was currently in remission.
However, the researchers caution that these alterations are not glaringly obvious on an individual level. “The differences were small,” Schmaal told PsyPost. “They are detectable because we were able to combine data from thousands of people, but they are nowhere near large enough to look at an individual person’s brain scan and determine whether they have taken antidepressants, or to use these measures in clinical decision-making.”
The differences between the medicated and unmedicated groups also vanished when the researchers accounted for the severity of current depressive symptoms. The people in the medicated group generally reported feeling worse at the time of the scan than the unmedicated group. This indicates that the structural differences in the temporal lobe and hippocampus might be tied more to how severely depressed a person is currently feeling, rather than being a direct physical result of the medication itself.
“We tried to account for factors such as current symptoms, number of previous depressive episodes and whether someone had recurrent depression, but it is impossible to completely separate medication use from illness severity in this kind of study,” Schmaal explained.
“Despite exploring every possible difference between those taking and those not taking antidepressants, there were only very small differences in very few brain areas which disappeared when taking into account other important differences between these groups,” Roland Zahn, a professor of Mood Disorders and Cognitive Neuroscience at King’s College London’s Centre for Affective Disorders who was not involved in the research, told PsyPost.
Zahn, who also serves as co-programme lead for the MSc Affective Disorders and shares research updates via his lab blog, added: “One important difference between the groups was that people taking antidepressants had much higher levels of depressive symptoms as measured on a gold standard observer-rated scale known to correlate with subtle changes in brain structure from other studies. When accounting for this crucial difference between the groups, the subtle differences in thickness of some of the brain areas in those taking antidepressants disappeared.”
The study also highlighted brain changes that seem driven by the depression diagnosis itself rather than the medication. Younger patients with depression, regardless of whether they took medication, had a smaller thalamus compared to healthy controls. The thalamus acts as a central relay station for sensory and motor signals in the brain. These younger patients also exhibited a thinner cortex in several regions across the frontal, occipital, and parietal lobes when compared to healthy individuals, a gap that was not present in the older participants.
In a smaller exploratory analysis, the researchers looked at specific types of antidepressants, comparing selective serotonin reuptake inhibitors (SSRIs), serotonin-norepinephrine reuptake inhibitors (SNRIs), and mirtazapine. They found an age-specific pattern here as well. Older adults (over the age of 40) taking mirtazapine had a thicker rostral anterior cingulate cortex compared to older adults taking SSRIs or SNRIs.
This brain region sits in the frontal lobe and is heavily involved in emotional regulation and reward processing. The authors suggest that mirtazapine might trigger a distinct neuroplastic response in this area, though they also note that mirtazapine is often prescribed for specific symptoms like insomnia or after other drugs have failed, which might influence the results.
“The authors acknowledge that they cannot establish causal relationships and particularly their comparison of different antidepressants is exploratory and based on a much smaller group, based on a single time point,” Zahn noted. “The problem is that there are several factors influencing the reason why someone is taking one antidepressant rather than another and the authors acknowledge, they were not able to account for that as this is a large study with limited clinical background information.”
The researchers also investigated how long patients had been on their current medication, finding no clear association between duration of use and structural changes. “We also did not find evidence that a longer duration of current antidepressant use was associated with greater brain differences,” Schmaal said. “That is reassuring in one sense, but it needs to be interpreted cautiously because detailed information on duration was available for only a subset of participants, and importantly we did not have people’s complete lifetime history of antidepressant exposure.”
The findings are in tension with research covered by PsyPost earlier this year, which found that patients taking the antidepressant escitalopram experienced increases in right hippocampal volume during their treatment. Both studies measure hippocampal volume via MRI in depressed patients taking antidepressants, but that earlier study tracked longitudinal within-person volume changes over weeks of treatment, whereas the new study assessed cross-sectional volume differences between different groups of medicated and unmedicated patients at a single point in time.
However, the ENIGMA study’s immense size adds significant weight to its findings. “This is a very important study in that it was able to merge data from thousands of people and therefore had the ability to detect very small differences,” Zahn said. “It thereby challenged findings from non-human animals as well as findings in smaller studies.”
As with all research, there are a few things to keep in mind. The study relies on a cross-sectional design, meaning the participants were only scanned once. Because the researchers did not track the same individuals over time, they cannot definitively say whether the antidepressants caused the observed brain differences, or if people with certain brain shapes and symptom severities are simply more likely to be prescribed antidepressants.
“The main misinterpretation I would want to avoid is that this study shows antidepressants cause the brain to shrink or cause brain damage. It does not,” Schmaal said. “Imagine taking a photograph of two groups of people today: one group taking antidepressants and another group not taking them. Even if their brains differ on average, that photograph cannot tell you what caused the difference or what their brains looked like before treatment.”
Zahn echoed this caution, emphasizing that brain anatomy is highly variable. “It is also important to note that the structure of our brains constantly changes and the biggest driver of such change is age,” he said. “It is also important to note that large individual differences in brain structure exist with little impact on functioning.”
Because of this limitation, the findings should not alter how patients currently manage their condition. “That is why these results should not be used to make decisions about starting or stopping antidepressants,” Schmaal added. “Those decisions need to be based on the balance of benefits and risks for an individual person and discussed with their treating clinician.”
The researchers also lacked data on the participants’ lifetime history of medication use, meaning some people in the “unmedicated” group might have taken antidepressants in the past. Other factors that shape brain anatomy over a lifespan, such as education, lifestyle habits, or early signs of neurodegenerative diseases in older adults, could not be fully accounted for across all 32 international sites.
“The next critical step is longitudinal research,” Schmaal told PsyPost. “Ideally, we need to follow people from before, or very soon after, they first start an antidepressant and repeatedly assess both their mental health and their brain over several years.”
“The next step as the authors acknowledge is to investigate multiple time points in datasets which contain more detail about other relevant factors, such as other conditions, and response to previous treatments,” Zahn added.
“Ultimately, the goal is not simply to ask whether antidepressants affect the brain,” Schmaal concluded. “We want to understand how they affect the developing and adult brain, whether those effects differ between individuals and across different ages, and whether any brain changes relate to treatment benefit, side effects or longer-term outcomes.”
The study, “Regional brain morphology and current antidepressant use: findings from 32 international cohorts from the ENIGMA major depressive disorder working group,” was authored by Chaira Serrarens, Yara J. Toenders, Elena Pozzi, André Aleman, Nina Alexander, Zeynep Başgöze, Vladimir Belov, Klaus Berger, Katharina Brosch, Robin Bülow, Geraldo Filho Busatto, Liliana P. Capitão, Colm G. Connolly, Baptiste Couvy-Duchesne, Kathryn R. Cullen, Udo Dannlowski, Christopher G. Davey, Greig I. de Zubicaray, Danai Dima, Katharina Dohm, Verena Enneking, Tracy Erwin-Grabner, Ulrika Evermann, Cynthia H. Y. Fu, Paola Fuentes-Claramonte, Beata R. Godlewska, Ali Saffet Gonul, Ian H. Gotlib, Roberto Goya-Maldonado, Hans J. Grabe, Nynke A. Groenewold, Dominik Grotegerd, Oliver Gruber, Tim Hahn, Geoffrey Hall, Ben J. Harrison, Walter Heindel, Marco Hermesdorf, Tiffany C. Ho, Naho Ichikawa, Eri Itai, Neda Jahanshad, Hamidreza Jamalabadi, Alec J. Jamieson, Andreas Jansen, Tilo Kircher, Bonnie Klimes-Dougan, Bernd Krämer, Axel Krug, Thomas M. Lancaster, Elisabeth J. Leehr, Meng Li, David E. J. Linden, Frank MacMaster, Katie L. McMahon, Sarah E. Medland, David M. A. Mehler, Susanne Meinert, Benson Mwangi, Igor Nenadić, Go Okada, Yasumasa Okamoto, Nils Opel, Julia-Katharina Pfarr, Edith Pomarol-Clotet, Maria J. Portella, Ronny Redlich, Liesbeth Reneman, Jonathan Repple, Kai Ringwald, Elena Rodriguez-Cano, Pedro G. P. Rosa, Matthew D. Sacchet, Philipp G. Sämann, Raymond Salvador, Anouk Schrantee, Hotaka Shinzato, Kang Sim, Egle Simulionyte, Jair C. Soares, Dan J. Stein, Frederike Stein, Benjamin Straube, Lachlan T. Strike, Florian Thomas-Odenthal, Sophia I. Thomopoulos, Paul M. Thompson, Marie-Jose van Tol, Paula Usemann, Aslihan Uyar, Nic van der Wee, Steven van der Werff, Yolanda Vives-Gilabert, Henry Völzke, Martin Walter, Sarah Whittle, Katharina Wittfeld, Adrian Wroblewski, Mon-Ju Wu, Tony T. Yang, Giovana B. Zunta-Soares, Dick J. Veltman, Lianne Schmaal, and Laura S. van Velzen.
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#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #antidepressants #brainstructure #ENIGMA #MDD #hippocampus #neuroimaging #MolecularPsychiatry #depressionresearch #lifespan #neuroplasticity
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"Oracle: Neuroplasticity"
Regeneration and adaptability. We can recover and rejuvenate from painful experiences. You already have what you need to change and grow; take it and turn it into something that serves the version of you that you want to be.#Watercolor #OracleDeck #JordanLynnGribbleArt #AbstractArt #Neuroplasticity
-
"Oracle: Neuroplasticity"
Regeneration and adaptability. We can recover and rejuvenate from painful experiences. You already have what you need to change and grow; take it and turn it into something that serves the version of you that you want to be.#Watercolor #OracleDeck #JordanLynnGribbleArt #AbstractArt #Neuroplasticity
-
"Oracle: Neuroplasticity"
Regeneration and adaptability. We can recover and rejuvenate from painful experiences. You already have what you need to change and grow; take it and turn it into something that serves the version of you that you want to be.#Watercolor #OracleDeck #JordanLynnGribbleArt #AbstractArt #Neuroplasticity
-
DATE: September 14, 2026 at 03:45AM
SOURCE: SOCIALPSYCHOLOGY.ORGTITLE: Hidden Brain Wiring May Keep Thinking Sharp As Gray Matter Shrinks
Source: Science Daily - Top News
A new study has uncovered evidence that two neighboring types of brain tissue may work together to support thinking abilities later in life. Its findings suggest that the condition of the brain's local communication pathways could influence how strongly gray matter loss affects cognition. The study, published in Alzheimer's & Dementia: The Journal of the Alzheimer's Association, was based on date from 459 adults aged 60 and older living in India.
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#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #HiddenBrainWiring #GrayMatterShrink #CognitionInAging #BrainConnectivity #AlzheimersResearch #Neuroplasticity #CognitiveReserve #AgingBrain #NeurologyNews #ScienceDaily
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DATE: September 14, 2026 at 03:45AM
SOURCE: SOCIALPSYCHOLOGY.ORGTITLE: Hidden Brain Wiring May Keep Thinking Sharp As Gray Matter Shrinks
Source: Science Daily - Top News
A new study has uncovered evidence that two neighboring types of brain tissue may work together to support thinking abilities later in life. Its findings suggest that the condition of the brain's local communication pathways could influence how strongly gray matter loss affects cognition. The study, published in Alzheimer's & Dementia: The Journal of the Alzheimer's Association, was based on date from 459 adults aged 60 and older living in India.
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#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #HiddenBrainWiring #GrayMatterShrink #CognitionInAging #BrainConnectivity #AlzheimersResearch #Neuroplasticity #CognitiveReserve #AgingBrain #NeurologyNews #ScienceDaily
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DATE: September 14, 2026 at 03:45AM
SOURCE: SOCIALPSYCHOLOGY.ORGTITLE: Hidden Brain Wiring May Keep Thinking Sharp As Gray Matter Shrinks
Source: Science Daily - Top News
A new study has uncovered evidence that two neighboring types of brain tissue may work together to support thinking abilities later in life. Its findings suggest that the condition of the brain's local communication pathways could influence how strongly gray matter loss affects cognition. The study, published in Alzheimer's & Dementia: The Journal of the Alzheimer's Association, was based on date from 459 adults aged 60 and older living in India.
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Private, vetted email list for mental health professionals: https://www.clinicians-exchange.org
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#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #HiddenBrainWiring #GrayMatterShrink #CognitionInAging #BrainConnectivity #AlzheimersResearch #Neuroplasticity #CognitiveReserve #AgingBrain #NeurologyNews #ScienceDaily
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DATE: September 14, 2026 at 10:23AM
SOURCE: SCIENCE DAILY MIND-BRAIN FEEDTITLE: Hidden brain wiring may help keep the mind sharp as gray matter shrinks
URL: https://www.sciencedaily.com/releases/2026/09/260913081921.htm
Scientists have discovered that the brain’s short-range wiring may help protect cognition even as gray matter shrinks with age. Healthier connections just beneath the brain’s surface were linked to better language skills and appeared to weaken the impact of gray matter loss.
URL: https://www.sciencedaily.com/releases/2026/09/260913081921.htm
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DATE: September 14, 2026 at 10:23AM
SOURCE: SCIENCE DAILY MIND-BRAIN FEEDTITLE: Hidden brain wiring may help keep the mind sharp as gray matter shrinks
URL: https://www.sciencedaily.com/releases/2026/09/260913081921.htm
Scientists have discovered that the brain’s short-range wiring may help protect cognition even as gray matter shrinks with age. Healthier connections just beneath the brain’s surface were linked to better language skills and appeared to weaken the impact of gray matter loss.
URL: https://www.sciencedaily.com/releases/2026/09/260913081921.htm
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-
DATE: September 14, 2026 at 10:23AM
SOURCE: SCIENCE DAILY MIND-BRAIN FEEDTITLE: Hidden brain wiring may help keep the mind sharp as gray matter shrinks
URL: https://www.sciencedaily.com/releases/2026/09/260913081921.htm
Scientists have discovered that the brain’s short-range wiring may help protect cognition even as gray matter shrinks with age. Healthier connections just beneath the brain’s surface were linked to better language skills and appeared to weaken the impact of gray matter loss.
URL: https://www.sciencedaily.com/releases/2026/09/260913081921.htm
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#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #BrainHealth #Cognition #AgingWell #GrayMatter #Neuroscience #MentalSharpness #BrainWiring #LanguageSkills #HealthyConnections #Neuroplasticity
-
Your brain is smarter and more adaptable than you think.
#BrainPower #Neuroplasticity #MindsetShift #GrowthMindset #UnlockYourPotential #ThinkandGrowEducation #RayBehan #Meditation #Frequencies -
Your brain is smarter and more adaptable than you think.
#BrainPower #Neuroplasticity #MindsetShift #GrowthMindset #UnlockYourPotential #ThinkandGrowEducation #RayBehan #Meditation #Frequencies -
Your brain is smarter and more adaptable than you think.
#BrainPower #Neuroplasticity #MindsetShift #GrowthMindset #UnlockYourPotential #ThinkandGrowEducation #RayBehan #Meditation #Frequencies -
Your brain is smarter and more adaptable than you think.
#BrainPower #Neuroplasticity #MindsetShift #GrowthMindset #UnlockYourPotential #ThinkandGrowEducation #RayBehan #Meditation #Frequencies -
DATE: September 4, 2026 at 06:00AM
SOURCE: PSYPOST.ORG** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
-------------------------------------------------TITLE: Regular coffee beats decaf in protecting the brain from chronic stress, mouse study finds
Regular coffee consumption might do more than just wake you up; it appears to protect the brain against the damaging effects of chronic stress. A new study in mice found that drinking caffeinated coffee prevented stress-induced memory loss and mood deterioration, while decaffeinated coffee offered no such benefits. The findings, published in Neurobiology of Stress, suggest that caffeine is the primary ingredient responsible for coffee’s mood-protecting properties.
For years, researchers have tried to understand the relationship between dietary habits and mental health. Epidemiological evidence frequently points to coffee as a protective beverage. For example, a study covered by PsyPost in 2026 indicated that moderate coffee consumption is associated with a lower risk of mood and stress disorders. These population studies raised an interesting question about which specific parts of the complex beverage drive these benefits.
Scientific investigations have built a case for caffeine as the active ingredient. As an example, a 2011 study of women found that drinking regular caffeinated coffee was linked to a lower risk of depression, whereas decaffeinated coffee offered no such protection. Following this, a 2015 study in mice demonstrated that pure caffeine prevents the mood and memory problems normally triggered by long-term stress. Yet, a 2018 analysis showed that decaf coffee still contains nearly all of the same healthy antioxidants as regular coffee, leaving scientists wondering if other nutrients in the beverage also played a role.
To settle whether caffeine is truly the essential ingredient for stress resilience, Ângelo R. Tomé and Rodrigo A. Cunha of the University of Coimbra led a research team to directly compare the effects of regular and decaffeinated coffee. They focused on how these beverages affected mice exposed to chronic unpredictable stress.
Chronic unpredictable stress is a laboratory model used to mimic human depression and anxiety. By exposing animals to mild, changing stressors over a period of several weeks, scientists can observe the resulting emotional and cognitive decline. The research team also wanted to look closely at changes in the brain, specifically measuring long-term potentiation and brain-derived neurotrophic factor.
Long-term potentiation is a process where the connections between neurons strengthen, serving as a cellular foundation for learning and memory. This activity is heavily concentrated in the hippocampus, a brain region dedicated to forming memories. Brain-derived neurotrophic factor is a protein that acts like a fertilizer for the brain, helping neurons grow and survive. The researchers measured this protein in the frontal cortex, an area heavily involved in complex behaviors and emotional regulation.
The research team studied 24 adult mice, dividing them into four groups. One group drank water and experienced no stress. The other three groups underwent three weeks of chronic unpredictable stress. During this time, they experienced random daily stressors, such as damp bedding, a brief cold bath, or having their cage tilted. One of the stressed groups drank regular water, another drank a caffeinated coffee extract, and the final group drank a decaffeinated coffee extract.
The mice received their respective beverages during their active nighttime hours, starting a week before the stress protocol began and continuing throughout the experiment. The amount of coffee the mice voluntarily drank roughly translated to an adult human consuming about 350 milligrams of caffeine a day, or roughly two to three standard cups of coffee.
Following the three weeks of stress, the researchers put the mice through a series of behavioral tests. They used an open field arena to measure spontaneous movement and general anxiety. They also evaluated anxiety by seeing how much time the mice spent in the unprotected open arms of an elevated maze. To assess depressive-like behaviors, the team observed the mice in a forced swimming test, recording how quickly they gave up struggling and simply floated.
The team sprayed a sticky sugar solution on the mice for a splash test, measuring how quickly they cleaned themselves as a sign of motivation and self-care. They also tracked whether the mice lost their natural preference for drinking a sweet sugar water solution. A loss of this preference serves as an indicator of anhedonia, which is the inability to feel pleasure.
Finally, the researchers tested spatial memory. They watched whether the mice could recognize when a familiar object had been moved to a new location in a testing arena. They also tested whether the mice preferred to explore a newly opened arm of a maze they had previously navigated.
The results showed that chronic unpredictable stress took a heavy toll on the mice drinking plain water. Compared to the unstressed controls, these mice lost weight, displayed heightened anxiety, and showed a pronounced lack of self-care. They also exhibited severe anhedonia, drinking much less sugar water than usual. Their spatial memory suffered, as they struggled to notice moved objects or explore new areas of the maze.
However, the mice that drank caffeinated coffee weathered the stress remarkably well. Their behavioral patterns were nearly identical to the control mice that experienced no stress at all. The caffeinated coffee prevented the weight loss, the anxiety, the despair in the swimming test, and the loss of motivation for self-care. It also fully protected their spatial memory.
The decaffeinated coffee failed to provide these robust protections. The stressed mice drinking decaf exhibited almost all the same behavioral deficits as the stressed mice drinking water. They failed to recover their body weight, remained anxious in the open field and maze tests, and showed persistent memory issues. While the decaf group showed very slight improvements in a few areas, these small changes were not statistically meaningful.
The brain tissue analysis provided a biological explanation for the behavioral differences. In the stressed mice drinking water, the magnitude of long-term potentiation in the hippocampus dropped from a roughly 61 percent baseline increase down to just 25 percent, indicating a severe disruption in memory-forming capacity. The levels of brain-derived neurotrophic factor in their frontal cortex also plummeted.
Drinking caffeinated coffee completely prevented these neurological declines. The mice in this group maintained normal long-term potentiation and normal levels of the neurotrophic protein, keeping their brain networks highly functional despite the chronic stress. Just as with the behavioral tests, decaffeinated coffee offered no protection for the brain, leaving the mice with diminished synaptic plasticity and depleted protein levels.
The findings are in line with research covered by PsyPost in 2024, which found that caffeine protects rodents from stress-induced spatial memory deficits and hippocampal impairment. They also align with a study covered by PsyPost in 2025, which demonstrated that caffeine prevents stress-induced depressive-like behaviors and preserves neurochemical balance in mice.
However, the results are in tension with another study covered by PsyPost in 2024. That study found that non-caffeine compounds in coffee protected against stress-induced cognitive deficits. It is worth noting that the earlier research tested isolated coffee polyphenols during early development, rather than using whole decaffeinated coffee in adult mice exposed to chronic stress, which likely explains the differing outcomes.
As with all research, there are a few things to keep in mind. The study did not measure the exact circulating levels of caffeine or other specific compounds in the blood or tissues of the mice. Because the animals were housed in small groups during the fluid consumption phase to avoid the added stress of isolation, the researchers could not track the precise individual intake for every single mouse.
The testing was also performed on a mixed group of male and female mice without isolating sex as a variable. Past studies suggest there may be discrete differences in how coffee impacts mood in males compared to females, which this study design could not explore. Finally, translating behavioral and brain changes from mice to humans always requires caution, as human diets, stress factors, and brain chemistry are far more complex.
The study, “Regular intake of caffeinated but not decaffeinated coffee attenuates behavioral modifications in mice subject to chronic unpredictable stress,” was authored by Ângelo R. Tomé, Nuno J. Machado, Ana Paula Ardais, Ana Nunes, Henrique B. Silva, Manuella P. Kaster, Paula Agostinho, and Rodrigo A. Cunha.
-------------------------------------------------
Private, vetted email list for mental health professionals: https://www.clinicians-exchange.org
Unofficial Psychology Today Xitter to toot feed at Psych Today Unofficial Bot @PTUnofficialBot
-------------------------------------------------
#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #coffee #caffeine #stressrelief #brainhealth #memory #mousestudy #neuroplasticity #hippocampus #anxiety #moodboost
-
DATE: September 4, 2026 at 06:00AM
SOURCE: PSYPOST.ORG** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
-------------------------------------------------TITLE: Regular coffee beats decaf in protecting the brain from chronic stress, mouse study finds
Regular coffee consumption might do more than just wake you up; it appears to protect the brain against the damaging effects of chronic stress. A new study in mice found that drinking caffeinated coffee prevented stress-induced memory loss and mood deterioration, while decaffeinated coffee offered no such benefits. The findings, published in Neurobiology of Stress, suggest that caffeine is the primary ingredient responsible for coffee’s mood-protecting properties.
For years, researchers have tried to understand the relationship between dietary habits and mental health. Epidemiological evidence frequently points to coffee as a protective beverage. For example, a study covered by PsyPost in 2026 indicated that moderate coffee consumption is associated with a lower risk of mood and stress disorders. These population studies raised an interesting question about which specific parts of the complex beverage drive these benefits.
Scientific investigations have built a case for caffeine as the active ingredient. As an example, a 2011 study of women found that drinking regular caffeinated coffee was linked to a lower risk of depression, whereas decaffeinated coffee offered no such protection. Following this, a 2015 study in mice demonstrated that pure caffeine prevents the mood and memory problems normally triggered by long-term stress. Yet, a 2018 analysis showed that decaf coffee still contains nearly all of the same healthy antioxidants as regular coffee, leaving scientists wondering if other nutrients in the beverage also played a role.
To settle whether caffeine is truly the essential ingredient for stress resilience, Ângelo R. Tomé and Rodrigo A. Cunha of the University of Coimbra led a research team to directly compare the effects of regular and decaffeinated coffee. They focused on how these beverages affected mice exposed to chronic unpredictable stress.
Chronic unpredictable stress is a laboratory model used to mimic human depression and anxiety. By exposing animals to mild, changing stressors over a period of several weeks, scientists can observe the resulting emotional and cognitive decline. The research team also wanted to look closely at changes in the brain, specifically measuring long-term potentiation and brain-derived neurotrophic factor.
Long-term potentiation is a process where the connections between neurons strengthen, serving as a cellular foundation for learning and memory. This activity is heavily concentrated in the hippocampus, a brain region dedicated to forming memories. Brain-derived neurotrophic factor is a protein that acts like a fertilizer for the brain, helping neurons grow and survive. The researchers measured this protein in the frontal cortex, an area heavily involved in complex behaviors and emotional regulation.
The research team studied 24 adult mice, dividing them into four groups. One group drank water and experienced no stress. The other three groups underwent three weeks of chronic unpredictable stress. During this time, they experienced random daily stressors, such as damp bedding, a brief cold bath, or having their cage tilted. One of the stressed groups drank regular water, another drank a caffeinated coffee extract, and the final group drank a decaffeinated coffee extract.
The mice received their respective beverages during their active nighttime hours, starting a week before the stress protocol began and continuing throughout the experiment. The amount of coffee the mice voluntarily drank roughly translated to an adult human consuming about 350 milligrams of caffeine a day, or roughly two to three standard cups of coffee.
Following the three weeks of stress, the researchers put the mice through a series of behavioral tests. They used an open field arena to measure spontaneous movement and general anxiety. They also evaluated anxiety by seeing how much time the mice spent in the unprotected open arms of an elevated maze. To assess depressive-like behaviors, the team observed the mice in a forced swimming test, recording how quickly they gave up struggling and simply floated.
The team sprayed a sticky sugar solution on the mice for a splash test, measuring how quickly they cleaned themselves as a sign of motivation and self-care. They also tracked whether the mice lost their natural preference for drinking a sweet sugar water solution. A loss of this preference serves as an indicator of anhedonia, which is the inability to feel pleasure.
Finally, the researchers tested spatial memory. They watched whether the mice could recognize when a familiar object had been moved to a new location in a testing arena. They also tested whether the mice preferred to explore a newly opened arm of a maze they had previously navigated.
The results showed that chronic unpredictable stress took a heavy toll on the mice drinking plain water. Compared to the unstressed controls, these mice lost weight, displayed heightened anxiety, and showed a pronounced lack of self-care. They also exhibited severe anhedonia, drinking much less sugar water than usual. Their spatial memory suffered, as they struggled to notice moved objects or explore new areas of the maze.
However, the mice that drank caffeinated coffee weathered the stress remarkably well. Their behavioral patterns were nearly identical to the control mice that experienced no stress at all. The caffeinated coffee prevented the weight loss, the anxiety, the despair in the swimming test, and the loss of motivation for self-care. It also fully protected their spatial memory.
The decaffeinated coffee failed to provide these robust protections. The stressed mice drinking decaf exhibited almost all the same behavioral deficits as the stressed mice drinking water. They failed to recover their body weight, remained anxious in the open field and maze tests, and showed persistent memory issues. While the decaf group showed very slight improvements in a few areas, these small changes were not statistically meaningful.
The brain tissue analysis provided a biological explanation for the behavioral differences. In the stressed mice drinking water, the magnitude of long-term potentiation in the hippocampus dropped from a roughly 61 percent baseline increase down to just 25 percent, indicating a severe disruption in memory-forming capacity. The levels of brain-derived neurotrophic factor in their frontal cortex also plummeted.
Drinking caffeinated coffee completely prevented these neurological declines. The mice in this group maintained normal long-term potentiation and normal levels of the neurotrophic protein, keeping their brain networks highly functional despite the chronic stress. Just as with the behavioral tests, decaffeinated coffee offered no protection for the brain, leaving the mice with diminished synaptic plasticity and depleted protein levels.
The findings are in line with research covered by PsyPost in 2024, which found that caffeine protects rodents from stress-induced spatial memory deficits and hippocampal impairment. They also align with a study covered by PsyPost in 2025, which demonstrated that caffeine prevents stress-induced depressive-like behaviors and preserves neurochemical balance in mice.
However, the results are in tension with another study covered by PsyPost in 2024. That study found that non-caffeine compounds in coffee protected against stress-induced cognitive deficits. It is worth noting that the earlier research tested isolated coffee polyphenols during early development, rather than using whole decaffeinated coffee in adult mice exposed to chronic stress, which likely explains the differing outcomes.
As with all research, there are a few things to keep in mind. The study did not measure the exact circulating levels of caffeine or other specific compounds in the blood or tissues of the mice. Because the animals were housed in small groups during the fluid consumption phase to avoid the added stress of isolation, the researchers could not track the precise individual intake for every single mouse.
The testing was also performed on a mixed group of male and female mice without isolating sex as a variable. Past studies suggest there may be discrete differences in how coffee impacts mood in males compared to females, which this study design could not explore. Finally, translating behavioral and brain changes from mice to humans always requires caution, as human diets, stress factors, and brain chemistry are far more complex.
The study, “Regular intake of caffeinated but not decaffeinated coffee attenuates behavioral modifications in mice subject to chronic unpredictable stress,” was authored by Ângelo R. Tomé, Nuno J. Machado, Ana Paula Ardais, Ana Nunes, Henrique B. Silva, Manuella P. Kaster, Paula Agostinho, and Rodrigo A. Cunha.
-------------------------------------------------
Private, vetted email list for mental health professionals: https://www.clinicians-exchange.org
Unofficial Psychology Today Xitter to toot feed at Psych Today Unofficial Bot @PTUnofficialBot
-------------------------------------------------
#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #coffee #caffeine #stressrelief #brainhealth #memory #mousestudy #neuroplasticity #hippocampus #anxiety #moodboost
-
DATE: September 4, 2026 at 06:00AM
SOURCE: PSYPOST.ORG** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
-------------------------------------------------TITLE: Regular coffee beats decaf in protecting the brain from chronic stress, mouse study finds
Regular coffee consumption might do more than just wake you up; it appears to protect the brain against the damaging effects of chronic stress. A new study in mice found that drinking caffeinated coffee prevented stress-induced memory loss and mood deterioration, while decaffeinated coffee offered no such benefits. The findings, published in Neurobiology of Stress, suggest that caffeine is the primary ingredient responsible for coffee’s mood-protecting properties.
For years, researchers have tried to understand the relationship between dietary habits and mental health. Epidemiological evidence frequently points to coffee as a protective beverage. For example, a study covered by PsyPost in 2026 indicated that moderate coffee consumption is associated with a lower risk of mood and stress disorders. These population studies raised an interesting question about which specific parts of the complex beverage drive these benefits.
Scientific investigations have built a case for caffeine as the active ingredient. As an example, a 2011 study of women found that drinking regular caffeinated coffee was linked to a lower risk of depression, whereas decaffeinated coffee offered no such protection. Following this, a 2015 study in mice demonstrated that pure caffeine prevents the mood and memory problems normally triggered by long-term stress. Yet, a 2018 analysis showed that decaf coffee still contains nearly all of the same healthy antioxidants as regular coffee, leaving scientists wondering if other nutrients in the beverage also played a role.
To settle whether caffeine is truly the essential ingredient for stress resilience, Ângelo R. Tomé and Rodrigo A. Cunha of the University of Coimbra led a research team to directly compare the effects of regular and decaffeinated coffee. They focused on how these beverages affected mice exposed to chronic unpredictable stress.
Chronic unpredictable stress is a laboratory model used to mimic human depression and anxiety. By exposing animals to mild, changing stressors over a period of several weeks, scientists can observe the resulting emotional and cognitive decline. The research team also wanted to look closely at changes in the brain, specifically measuring long-term potentiation and brain-derived neurotrophic factor.
Long-term potentiation is a process where the connections between neurons strengthen, serving as a cellular foundation for learning and memory. This activity is heavily concentrated in the hippocampus, a brain region dedicated to forming memories. Brain-derived neurotrophic factor is a protein that acts like a fertilizer for the brain, helping neurons grow and survive. The researchers measured this protein in the frontal cortex, an area heavily involved in complex behaviors and emotional regulation.
The research team studied 24 adult mice, dividing them into four groups. One group drank water and experienced no stress. The other three groups underwent three weeks of chronic unpredictable stress. During this time, they experienced random daily stressors, such as damp bedding, a brief cold bath, or having their cage tilted. One of the stressed groups drank regular water, another drank a caffeinated coffee extract, and the final group drank a decaffeinated coffee extract.
The mice received their respective beverages during their active nighttime hours, starting a week before the stress protocol began and continuing throughout the experiment. The amount of coffee the mice voluntarily drank roughly translated to an adult human consuming about 350 milligrams of caffeine a day, or roughly two to three standard cups of coffee.
Following the three weeks of stress, the researchers put the mice through a series of behavioral tests. They used an open field arena to measure spontaneous movement and general anxiety. They also evaluated anxiety by seeing how much time the mice spent in the unprotected open arms of an elevated maze. To assess depressive-like behaviors, the team observed the mice in a forced swimming test, recording how quickly they gave up struggling and simply floated.
The team sprayed a sticky sugar solution on the mice for a splash test, measuring how quickly they cleaned themselves as a sign of motivation and self-care. They also tracked whether the mice lost their natural preference for drinking a sweet sugar water solution. A loss of this preference serves as an indicator of anhedonia, which is the inability to feel pleasure.
Finally, the researchers tested spatial memory. They watched whether the mice could recognize when a familiar object had been moved to a new location in a testing arena. They also tested whether the mice preferred to explore a newly opened arm of a maze they had previously navigated.
The results showed that chronic unpredictable stress took a heavy toll on the mice drinking plain water. Compared to the unstressed controls, these mice lost weight, displayed heightened anxiety, and showed a pronounced lack of self-care. They also exhibited severe anhedonia, drinking much less sugar water than usual. Their spatial memory suffered, as they struggled to notice moved objects or explore new areas of the maze.
However, the mice that drank caffeinated coffee weathered the stress remarkably well. Their behavioral patterns were nearly identical to the control mice that experienced no stress at all. The caffeinated coffee prevented the weight loss, the anxiety, the despair in the swimming test, and the loss of motivation for self-care. It also fully protected their spatial memory.
The decaffeinated coffee failed to provide these robust protections. The stressed mice drinking decaf exhibited almost all the same behavioral deficits as the stressed mice drinking water. They failed to recover their body weight, remained anxious in the open field and maze tests, and showed persistent memory issues. While the decaf group showed very slight improvements in a few areas, these small changes were not statistically meaningful.
The brain tissue analysis provided a biological explanation for the behavioral differences. In the stressed mice drinking water, the magnitude of long-term potentiation in the hippocampus dropped from a roughly 61 percent baseline increase down to just 25 percent, indicating a severe disruption in memory-forming capacity. The levels of brain-derived neurotrophic factor in their frontal cortex also plummeted.
Drinking caffeinated coffee completely prevented these neurological declines. The mice in this group maintained normal long-term potentiation and normal levels of the neurotrophic protein, keeping their brain networks highly functional despite the chronic stress. Just as with the behavioral tests, decaffeinated coffee offered no protection for the brain, leaving the mice with diminished synaptic plasticity and depleted protein levels.
The findings are in line with research covered by PsyPost in 2024, which found that caffeine protects rodents from stress-induced spatial memory deficits and hippocampal impairment. They also align with a study covered by PsyPost in 2025, which demonstrated that caffeine prevents stress-induced depressive-like behaviors and preserves neurochemical balance in mice.
However, the results are in tension with another study covered by PsyPost in 2024. That study found that non-caffeine compounds in coffee protected against stress-induced cognitive deficits. It is worth noting that the earlier research tested isolated coffee polyphenols during early development, rather than using whole decaffeinated coffee in adult mice exposed to chronic stress, which likely explains the differing outcomes.
As with all research, there are a few things to keep in mind. The study did not measure the exact circulating levels of caffeine or other specific compounds in the blood or tissues of the mice. Because the animals were housed in small groups during the fluid consumption phase to avoid the added stress of isolation, the researchers could not track the precise individual intake for every single mouse.
The testing was also performed on a mixed group of male and female mice without isolating sex as a variable. Past studies suggest there may be discrete differences in how coffee impacts mood in males compared to females, which this study design could not explore. Finally, translating behavioral and brain changes from mice to humans always requires caution, as human diets, stress factors, and brain chemistry are far more complex.
The study, “Regular intake of caffeinated but not decaffeinated coffee attenuates behavioral modifications in mice subject to chronic unpredictable stress,” was authored by Ângelo R. Tomé, Nuno J. Machado, Ana Paula Ardais, Ana Nunes, Henrique B. Silva, Manuella P. Kaster, Paula Agostinho, and Rodrigo A. Cunha.
-------------------------------------------------
Private, vetted email list for mental health professionals: https://www.clinicians-exchange.org
Unofficial Psychology Today Xitter to toot feed at Psych Today Unofficial Bot @PTUnofficialBot
-------------------------------------------------
#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #coffee #caffeine #stressrelief #brainhealth #memory #mousestudy #neuroplasticity #hippocampus #anxiety #moodboost
-
DATE: September 4, 2026 at 06:00AM
SOURCE: PSYPOST.ORG** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
-------------------------------------------------TITLE: Regular coffee beats decaf in protecting the brain from chronic stress, mouse study finds
Regular coffee consumption might do more than just wake you up; it appears to protect the brain against the damaging effects of chronic stress. A new study in mice found that drinking caffeinated coffee prevented stress-induced memory loss and mood deterioration, while decaffeinated coffee offered no such benefits. The findings, published in Neurobiology of Stress, suggest that caffeine is the primary ingredient responsible for coffee’s mood-protecting properties.
For years, researchers have tried to understand the relationship between dietary habits and mental health. Epidemiological evidence frequently points to coffee as a protective beverage. For example, a study covered by PsyPost in 2026 indicated that moderate coffee consumption is associated with a lower risk of mood and stress disorders. These population studies raised an interesting question about which specific parts of the complex beverage drive these benefits.
Scientific investigations have built a case for caffeine as the active ingredient. As an example, a 2011 study of women found that drinking regular caffeinated coffee was linked to a lower risk of depression, whereas decaffeinated coffee offered no such protection. Following this, a 2015 study in mice demonstrated that pure caffeine prevents the mood and memory problems normally triggered by long-term stress. Yet, a 2018 analysis showed that decaf coffee still contains nearly all of the same healthy antioxidants as regular coffee, leaving scientists wondering if other nutrients in the beverage also played a role.
To settle whether caffeine is truly the essential ingredient for stress resilience, Ângelo R. Tomé and Rodrigo A. Cunha of the University of Coimbra led a research team to directly compare the effects of regular and decaffeinated coffee. They focused on how these beverages affected mice exposed to chronic unpredictable stress.
Chronic unpredictable stress is a laboratory model used to mimic human depression and anxiety. By exposing animals to mild, changing stressors over a period of several weeks, scientists can observe the resulting emotional and cognitive decline. The research team also wanted to look closely at changes in the brain, specifically measuring long-term potentiation and brain-derived neurotrophic factor.
Long-term potentiation is a process where the connections between neurons strengthen, serving as a cellular foundation for learning and memory. This activity is heavily concentrated in the hippocampus, a brain region dedicated to forming memories. Brain-derived neurotrophic factor is a protein that acts like a fertilizer for the brain, helping neurons grow and survive. The researchers measured this protein in the frontal cortex, an area heavily involved in complex behaviors and emotional regulation.
The research team studied 24 adult mice, dividing them into four groups. One group drank water and experienced no stress. The other three groups underwent three weeks of chronic unpredictable stress. During this time, they experienced random daily stressors, such as damp bedding, a brief cold bath, or having their cage tilted. One of the stressed groups drank regular water, another drank a caffeinated coffee extract, and the final group drank a decaffeinated coffee extract.
The mice received their respective beverages during their active nighttime hours, starting a week before the stress protocol began and continuing throughout the experiment. The amount of coffee the mice voluntarily drank roughly translated to an adult human consuming about 350 milligrams of caffeine a day, or roughly two to three standard cups of coffee.
Following the three weeks of stress, the researchers put the mice through a series of behavioral tests. They used an open field arena to measure spontaneous movement and general anxiety. They also evaluated anxiety by seeing how much time the mice spent in the unprotected open arms of an elevated maze. To assess depressive-like behaviors, the team observed the mice in a forced swimming test, recording how quickly they gave up struggling and simply floated.
The team sprayed a sticky sugar solution on the mice for a splash test, measuring how quickly they cleaned themselves as a sign of motivation and self-care. They also tracked whether the mice lost their natural preference for drinking a sweet sugar water solution. A loss of this preference serves as an indicator of anhedonia, which is the inability to feel pleasure.
Finally, the researchers tested spatial memory. They watched whether the mice could recognize when a familiar object had been moved to a new location in a testing arena. They also tested whether the mice preferred to explore a newly opened arm of a maze they had previously navigated.
The results showed that chronic unpredictable stress took a heavy toll on the mice drinking plain water. Compared to the unstressed controls, these mice lost weight, displayed heightened anxiety, and showed a pronounced lack of self-care. They also exhibited severe anhedonia, drinking much less sugar water than usual. Their spatial memory suffered, as they struggled to notice moved objects or explore new areas of the maze.
However, the mice that drank caffeinated coffee weathered the stress remarkably well. Their behavioral patterns were nearly identical to the control mice that experienced no stress at all. The caffeinated coffee prevented the weight loss, the anxiety, the despair in the swimming test, and the loss of motivation for self-care. It also fully protected their spatial memory.
The decaffeinated coffee failed to provide these robust protections. The stressed mice drinking decaf exhibited almost all the same behavioral deficits as the stressed mice drinking water. They failed to recover their body weight, remained anxious in the open field and maze tests, and showed persistent memory issues. While the decaf group showed very slight improvements in a few areas, these small changes were not statistically meaningful.
The brain tissue analysis provided a biological explanation for the behavioral differences. In the stressed mice drinking water, the magnitude of long-term potentiation in the hippocampus dropped from a roughly 61 percent baseline increase down to just 25 percent, indicating a severe disruption in memory-forming capacity. The levels of brain-derived neurotrophic factor in their frontal cortex also plummeted.
Drinking caffeinated coffee completely prevented these neurological declines. The mice in this group maintained normal long-term potentiation and normal levels of the neurotrophic protein, keeping their brain networks highly functional despite the chronic stress. Just as with the behavioral tests, decaffeinated coffee offered no protection for the brain, leaving the mice with diminished synaptic plasticity and depleted protein levels.
The findings are in line with research covered by PsyPost in 2024, which found that caffeine protects rodents from stress-induced spatial memory deficits and hippocampal impairment. They also align with a study covered by PsyPost in 2025, which demonstrated that caffeine prevents stress-induced depressive-like behaviors and preserves neurochemical balance in mice.
However, the results are in tension with another study covered by PsyPost in 2024. That study found that non-caffeine compounds in coffee protected against stress-induced cognitive deficits. It is worth noting that the earlier research tested isolated coffee polyphenols during early development, rather than using whole decaffeinated coffee in adult mice exposed to chronic stress, which likely explains the differing outcomes.
As with all research, there are a few things to keep in mind. The study did not measure the exact circulating levels of caffeine or other specific compounds in the blood or tissues of the mice. Because the animals were housed in small groups during the fluid consumption phase to avoid the added stress of isolation, the researchers could not track the precise individual intake for every single mouse.
The testing was also performed on a mixed group of male and female mice without isolating sex as a variable. Past studies suggest there may be discrete differences in how coffee impacts mood in males compared to females, which this study design could not explore. Finally, translating behavioral and brain changes from mice to humans always requires caution, as human diets, stress factors, and brain chemistry are far more complex.
The study, “Regular intake of caffeinated but not decaffeinated coffee attenuates behavioral modifications in mice subject to chronic unpredictable stress,” was authored by Ângelo R. Tomé, Nuno J. Machado, Ana Paula Ardais, Ana Nunes, Henrique B. Silva, Manuella P. Kaster, Paula Agostinho, and Rodrigo A. Cunha.
-------------------------------------------------
Private, vetted email list for mental health professionals: https://www.clinicians-exchange.org
Unofficial Psychology Today Xitter to toot feed at Psych Today Unofficial Bot @PTUnofficialBot
-------------------------------------------------
#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #coffee #caffeine #stressrelief #brainhealth #memory #mousestudy #neuroplasticity #hippocampus #anxiety #moodboost
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#Storytelling #NarrativeLearning #KnowledgeOrganization #HumanLearning #PowerOfStories #StorytellingTechniques #EducationalVideo #LearningStrategies #NarrativeStructure #NeuroScience #NeuroDivergent #NeuroCiencia #Neuro #Neurology #NeuroSurgery #NeuroPlasticity #NeuroCirurgia #ThePowerOfNarrative https://mastodon.social/@biohackingpathway/117173515213512458
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#GoodMorningText #RelationshipGoals #Connection #MorningMotivation #PositiveVibes #MentalHealth #EmotionalWellbeing #SelfCare #Community #NeuroPlasticity #NeuroCirurgia #NeuroDiverse #NeuroFeedback #Neuropathy #NeuroSurgeon #NeuroDiversidade #NeuroPsychology #Tribe https://mastodon.social/@biohackingpathway/117125463550786183
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Your Brain is 1/200th Plastic 🤯🤔
#Biohacking #BrainHealth #Neuroplasticity #MindOverMatter #BrainOptimization #MentalWellbeing #SelfImprovement #HealthHacks #WellnessJourney #Mindfulness #CognitiveEnhancement #HealthyLiving #BrainTraining #MentalClarity #HolisticHealth -
Your Brain is 1/200th Plastic 🤯🤔
#Biohacking #BrainHealth #Neuroplasticity #MindOverMatter #BrainOptimization #MentalWellbeing #SelfImprovement #HealthHacks #WellnessJourney #Mindfulness #CognitiveEnhancement #HealthyLiving #BrainTraining #MentalClarity #HolisticHealth -
Your Brain is 1/200th Plastic 🤯🤔
#Biohacking #BrainHealth #Neuroplasticity #MindOverMatter #BrainOptimization #MentalWellbeing #SelfImprovement #HealthHacks #WellnessJourney #Mindfulness #CognitiveEnhancement #HealthyLiving #BrainTraining #MentalClarity #HolisticHealth -
Your Brain is 1/200th Plastic 🤯🤔
#Biohacking #BrainHealth #Neuroplasticity #MindOverMatter #BrainOptimization #MentalWellbeing #SelfImprovement #HealthHacks #WellnessJourney #Mindfulness #CognitiveEnhancement #HealthyLiving #BrainTraining #MentalClarity #HolisticHealth -
I rewired my brain by changing what I repeated daily.
https://elite.thinkandgroweducation.com.au/feed-336-7.html
#RewireYourBrain #MindsetShift #Neuroplasticity #PersonalGrowth #InnerTransformation #ThinkandGrowEducation #RayBehan #Neuroplasticity #Science -
I rewired my brain by changing what I repeated daily.
https://elite.thinkandgroweducation.com.au/feed-336-7.html
#RewireYourBrain #MindsetShift #Neuroplasticity #PersonalGrowth #InnerTransformation #ThinkandGrowEducation #RayBehan #Neuroplasticity #Science -
I rewired my brain by changing what I repeated daily.
https://elite.thinkandgroweducation.com.au/feed-336-7.html
#RewireYourBrain #MindsetShift #Neuroplasticity #PersonalGrowth #InnerTransformation #ThinkandGrowEducation #RayBehan #Neuroplasticity #Science -
I rewired my brain by changing what I repeated daily.
https://elite.thinkandgroweducation.com.au/feed-336-7.html
#RewireYourBrain #MindsetShift #Neuroplasticity #PersonalGrowth #InnerTransformation #ThinkandGrowEducation #RayBehan #Neuroplasticity #Science -
Harnessing Brain Plasticity: Strategies for Lifelong Learning and Personal Growth
Photo by KATRIN BOLOVTSOVA on Pexels.com Brain plasticity means your brain can change and grow at any age. (Margetis & Vadakekut, 2026) Whether you’re picking up a new language or dealing with life changes, adults can learn just like kids do. This adaptability is super helpful when life's big shifts happen. When you practice or start thinking differently, your brain makes new connections. This means even adult brains can create new cells that help with memory. If you make it a habit, you […] -
Ayant oublié de glisser ce point lors de mon dernier Nexus, je publie l'information ici.
Tout le monde connait la molécule Zolpidem (3), un puissant hypnotique de la famille des Imidazopyridines, aux effets plus ou moins proches des BZD. Or, peu connaissent (incluant les médecins) les effets spectaculaires de neuroplasticité que cet incontournable somnifère renferme.
En 1999, en Afrique du Sud, un medecin arrive à ramener, de façon fortuite, un patient comateux à l'état de veille par administration de Zolpidem.
De là, durant des années, loin des tabloïds, des essais furent effectués sur des personnes atteintes de lésions cérébrales, permettant de démontrer l'action majeure de ce PA à l'impressionnant rétablissement des fonctions cerebrales atteintes (post-AVC, Traumatisme Cranien, Hypoxie, etc.) (1). Nommé "Effet Ambien" (du nom américain de la molecule). Pour constater l'effet bluffant de ces rétablissements, Hamilton Morris avait fait, en 2013, un excellent reportage sur le sujet (en bas ce ce message).
Encore l'année dernière, dans un silence absolu, une publication détaillait l'efficacité thérapeutique du Zolpidem sur les cas de catatonie (2).
Pour son mécanisme Biochimique, plusieurs hypothèses sont encore en discussion :
- Hypothèse de la Dormance Cérébrale -> Certaines zones cérébrales lésées ne sont pas mortes, mais en état de dormance. Une perfusion observée après l'administration de Zolpidem.
- Hypothèse MesoCircuit -> Inhibition directe du GPi et restauration thalamique
- Hypothèse de la Signalisation Phasique vs Tonique
Une dernière chose troublante. Contrairement à ce que nous pourrions penser, alors qu'une prise de Zolpidem plonge quiconque dans un sommeil indiscutable, les personnes atteintes d'affres cérébrales prenant ce PA ne ressentent aucune sensation de sommeil. Cette magie s'opére par l'effet agoniste sélectif des récepteurs GABAₐ-α1, sous-type ω1, qui au contact de récepteurs GABA "normaux" joueraient leur role naturel de somnifère, et en présence de récepteurs "anormaux" (dans le cas d'atteintes cérébrales) les modifieraient pour les rétablir.
youtu.be/KTFicgrVk0w
(1) : doi.org/10.1080/02699052.2017.1300836
(2) : www.sciencedirect.com/science/article/abs/pii/S2667296024001149
(3) : pubchem.ncbi.nlm.nih.gov/compound/Zolpidem-tartrate
#FolkPharmacology #pharmacology #Zolpidem #Neurosciences #neuroplasticity #psychedelics
Cc : @denissalem @tcrouzet @beanface42 @dlb -
Your Brain in the Age of AI: How to Keep Growing When a Machine Can Think for You
Claire noticed it about four months into using AI for nearly everything — the reports, the client summaries, the first drafts of pitches she used to sweat over for hours. Her output had gotten faster. Cleaner, even. Nobody on her team could tell the difference between what she'd written and what the machine had drafted for her, and honestly, neither could she anymore. What she couldn't figure out was David. David sat two desks over, ran the same tools she did, and by any reasonable […]https://www.acumentor.co/sustaining-intellectual-growth-age-of-ai/
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#stressmanagement #emotionalhealth #mentalhealth #wellbeing #healthylifestyle #stressrelief #emotionalregulation #mindbodyspirit #NeuroScience #NeuroDivergent #NeuroCiencia #Neuro #Neurology #NeuroSurgery #NeuroPlasticity #NeuroCirurgia #selfcare https://mastodon.social/@biohackingpathway/117012161175825702
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#BrainwaveCoherence #AutonomicNervousSystem #Biofeedback #HolisticHealth #MindBodyConnection #Neurocience #Wellbeing #Neuro #Neurology #NeuroSurgery #NeuroPlasticity #NeuroCirurgia #NeuroDiverse #NeuroFeedback #Neuropathy #NeuroSurgeon #NeuroDiversidade #NeuroPsychology #BrainHealth #StressManagement https://mastodon.social/@biohackingpathway/117006503676025801
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Fear is often just a pattern your brain has practiced too many times.
https://de320.isrefer.com/go/LUYDFREE/Stuartn/
#UnwireYourFear #MindsetShift #FearToFreedom #RewireYourBrain #InnerStrength #ThinkandGrowEducation #RayBehan #Fear #Neuroplasticity -
💁🏻♀️ TIL: 🦇🧠 A 2021 study found #blind and sighted people can learn click #echolocation in just 10 weeks.
Follow up scans by #Durham University researchers showed structural changes in the #brain’s visual cortex. A separate 2025 study examined how 30 million years of echolocation #evolution shaped dolphin and whale brains.
👉 https://www.sciencealert.com/humans-can-echolocate-and-it-changes-the-wiring-of-the-brain
#neuroplasticity #science #biology #humanbody #sound #adaptation #learning #neuroscience #dolphins #whales #disability #humans #animals #bats
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💁🏻♀️ TIL: 🦇🧠 A 2021 study found #blind and sighted people can learn click #echolocation in just 10 weeks.
Follow up scans by #Durham University researchers showed structural changes in the #brain’s visual cortex. A separate 2025 study examined how 30 million years of echolocation #evolution shaped dolphin and whale brains.
👉 https://www.sciencealert.com/humans-can-echolocate-and-it-changes-the-wiring-of-the-brain
#neuroplasticity #science #biology #humanbody #sound #adaptation #learning #neuroscience #dolphins #whales #disability #humans #animals #bats
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💁🏻♀️ TIL: 🦇🧠 A 2021 study found #blind and sighted people can learn click #echolocation in just 10 weeks.
Follow up scans by #Durham University researchers showed structural changes in the #brain’s visual cortex. A separate 2025 study examined how 30 million years of echolocation #evolution shaped dolphin and whale brains.
👉 https://www.sciencealert.com/humans-can-echolocate-and-it-changes-the-wiring-of-the-brain
#neuroplasticity #science #biology #humanbody #sound #adaptation #learning #neuroscience #dolphins #whales #disability #humans #animals #bats
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💁🏻♀️ TIL: 🦇🧠 A 2021 study found #blind and sighted people can learn click #echolocation in just 10 weeks.
Follow up scans by #Durham University researchers showed structural changes in the #brain’s visual cortex. A separate 2025 study examined how 30 million years of echolocation #evolution shaped dolphin and whale brains.
👉 https://www.sciencealert.com/humans-can-echolocate-and-it-changes-the-wiring-of-the-brain
#neuroplasticity #science #biology #humanbody #sound #adaptation #learning #neuroscience #dolphins #whales #disability #humans #animals #bats
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ECT Reprograms Adult Neurons into a Youthful State
Summary: Researchers engineered a highly specialized patterned stimulation protocol called REPOPS (Repeated Electroconvulsive-like Patterned Optical/Electrical Stimulation) in murine…
#NewsBeep #News #Health #brainplasticity #brainresearch #ECT #elecrophysiology #electroconvulsivetherapy #FujitaHealthUniversity #GB #neurobiology #neuroplasticity #Neuroscience #Neurotech #synapticplasticity #UK #UnitedKingdom
https://www.newsbeep.com/uk/699357/ -
Exercise Redefines Heart Nerve Networks, Offering New Treatment Insights
📰 Original title: Exercise doesn't just strengthen the heart. It rewires it
🤖 IA: It's not clickbait ✅
👥 Users: It's not clickbait ✅View full AI summary https://en.killbait.com/exercise-redefines-heart-nerve-networks-offering-new-treatment-insights.html?utm_source=mastodon_world&utm_medium=social&utm_campaign=killbait.mastodon_world
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Every time you learn something new, your brain literally reshapes itself.
https://de320.isrefer.com/go/root396gift/Stuartn/
#Neuroplasticity #LearningChangesYou #GrowthMindset #BrainPower #InnerTransformation #ThinkandGrowEducation #RayBehan #Neuroplasticity #RewiringtheBrain -
Your brain doesn’t just find answers it filters for the ones it expects to see.
https://de320.isrefer.com/go/LUYDFREE/Stuartn/
#MindsetShift #BrainPower #PerceptionMatters #Neuroplasticity #AskBetterQuestions #InnerTransformation #ThinkandGrowEducation #RayBehan #LeftBrain #RightBrain -
Neuroplasticity doesn't care about your ideal of a quiet mind. It responds to repeated patterns. Each time you notice you've drifted and gently return, you're strengthening the neural circuits of attention and self-regulation. The 'kindness' part is what prevents the amygdala from hijacking the loop. That's the boring, effective science.
https://www.udemy.com/course/positive-psychology-mastering-resilience-mindfulness-n
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Myelination is how repetition becomes power.
https://de320.isrefer.com/go/root396gift/Stuartn/
#Myelination #BrainTraining #Neuroplasticity #HabitChange #PersonalGrowth #MindsetShift #ThinkandGrowEducation #RayBehan #Meditation -
Myelination is how repetition becomes power.
https://de320.isrefer.com/go/root396gift/Stuartn/
#Myelination #BrainTraining #Neuroplasticity #HabitChange #PersonalGrowth #MindsetShift #ThinkandGrowEducation #RayBehan #Meditation -
Your brain is smarter and more adaptable than you think.
https://de320.isrefer.com/go/root396gift/Stuartn/
#BrainPower #LimitlessPotential #Neuroplasticity #EmbraceGrowth #UnlockYourMind #SmartThinking #ThinkandGrowEducation #RayBehan #Meditation #RewiringYourBrain -
Your brain is smarter and more adaptable than you think.
https://de320.isrefer.com/go/root396gift/Stuartn/
#BrainPower #LimitlessPotential #Neuroplasticity #EmbraceGrowth #UnlockYourMind #SmartThinking #ThinkandGrowEducation #RayBehan #Meditation #RewiringYourBrain -
Rewiring your brain is powerful and possible.
https://de320.isrefer.com/go/UNTHINKABLE/Stuartn/
#RewireYourBrain #Neuroplasticity #GrowthMindset #BrainTraining #LimitlessPotential #MindsetShift #ThinkandGrowEducation #RayBehan #NewInformation #UNTHINKABLE -
Magic mushrooms and Alzheimer’s: what one remarkable case can tell us
#Health #Alzheimers #Dementia #Psilocybin #BrainHealth #MagicMushrooms #Neuroscience #MentalHealthResearch #Neuroplasticity #MedicalResearch #MagicMushrooms
https://the-14.com/magic-mushrooms-and-alzheimers-what-one-remarkable-case-can-tell-us/